ECE2020 Audio ePoster Presentations Bone and Calcium (121 abstracts)
1KULeuven, Department of Chronic Diseases, Metabolism and Ageing (CHROMETA), Laboratory of Clinical and Experimental Endocrinology, Leuven, Belgium; 2University Hospitals Leuven, Department of Endocrinology, Leuven, Belgium; 3Rigshospitalet, University Department of Growth and Reproduction, Copenhagen, Denmark; 4Rigshospitalet, International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Copenhagen, Denmark
Background: Male infertility is associated with a higher long-term morbidity and mortality risk. However, it is not clear which diseases are contributing to this risk. Osteoporosis is a possible factor, as it is a frequent disease and sex steroids regulate both fertility and bone health. Furthermore, there are data indicating that high FSH levels in women are related to low bone mineral density (BMD), independent of estradiol levels. As infertile men often have increased FSH, already from a young age, this could be a risk factor for impaired bone health in later life.
Methods: One hundred and thirty-seven men with a history of male factor infertility due to spermatogenic failure (SgF men) as well as a control group of 70 men from couples treated with IVF for female factor infertility (non-SgF men) were included in a long-term follow-up study. Men with explained infertility, including testosterone deficiency, were excluded. Data from baseline fertility investigations were retrieved from the patient files of the SgF men. At follow-up, hormonal and semen analysis was performed and axial, femoral and total body BMD was measured by dual X-ray absorptiometryin all men. Multiple linear regression was used to assess differences between SgF and non-SgF men and to study associations between FSH levels and BMD.
Results: Median follow-up time was 14.8 years (5th-95th percentile 11.3–18.2) after fertility assessment for SgF men and 15.6 years (12.1–18.5) for non-SgF men (p = 0.033). When comparing the two groups, no significant differences in total T, free T or E2 levels were apparent at follow-up. As expected, LH and FSH were higher in SgF men (median (5th–95th percentile)) for LH (IU/l): 4.3 (2.2–13.6) for SgF men and 3.0 (1.4–5.8) for non-SgF men (P <0.001); FSH (IU/l): 9.8 (2.8–35.5) vs 3.7 (1.6–8.7); P < 0.001). Inhibin B and semen parameters were lower in SgF men.
There were no differences in BMD between the two groups. Furthermore, both groups had median Z-scores close to zero at all sites, indicating that BMD is not different when compared to age-matched healthy men. In SgF men, neither baseline FSH, nor FSH at follow-up, was associated with BMD at the different sites at follow-up.
Conclusion: Men with spermatogenic failure are not at increased risk for impaired bone health later in life. Furthermore, infertile men with high FSH levels do not have lower BMD.